Catatonia Yesterday, Today, Tomorrow

Transcription

1 Western University Psychiatry Presentations Psychiatry Department Catatonia Yesterday, Today, Tomorrow Amresh Srivastava University of Western Ontario, Follow this and additional works at: Part of the Psychiatry and Psychology Commons Citation of this paper: Srivastava, Amresh, "Catatonia Yesterday, Today, Tomorrow" (2007). Psychiatry Presentations

2 Catatonia Yesterday, today, tomorrow Amresh Shrivastava Assistant Professor University of western Ontario, London, Canada & Physician Team leader, Early psychosis Programme, RMHC- St.Thomas 15th, January 2007 Amresh Srivastava, 1

3 Disappearance vs.. re-emergence Challenging, High mortality Life-threatening Beyond psychiatry Offers interface with medicine and neurology Constantly evolving in understanding 52 publications in th, January 2007 Amresh Srivastava, 2

4 Catatonia: Case vintage. A 40-yr.old man treated for psychosis with antipsychotic and antimanic medications since age of 16, was attending a community clinic, and stabilized with lithiumand chlorpromazine therapy. Encouraged by stability of condition therapist prescribed olazapine. Within a few weeks patient again became psychotic. Perphanizine was prescribed, within a day he became febrile, mute and rigid. Hospitalized and diagnosed as NMS, transferred to tertiary care facility APD was discontinued, further treated with large doses of bromochriptine & dantrolene. Repetitive movements prompted diagnosis of epilepsy, so anticonvulsants were administered. Lorazepam prescribed in low dose controlled infrequent agitation but he remained mute and rigid, required total nursing care After few weeks he was unable to stand; hands and legs were in rigid, immobile posture. A gastrostomy was done to permit feeding, he developed pulmonary and bladder infection requiring antibiotics He spent four months in intensive medical care and after that a visiting consultant [psychiatrist] recommended lorazepam in high doses. When the daily dose was increased to 12mg he responded to commands and smiled at his parents, though he remained mute ECT was recommended but the hospital had no facility, so he was transferred When his mother was signing the consent for ECT she recalled that he had a similar episode of rigidity mutism and psychosis at 16 years of age and responded to ECT 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 3

5 Lorazepam was reduced to 6 mgs per day and bilateral ECT begun After 4 treatments he recognized his parents, vocalized, smiled, was less rigid and took oral feedings By 9 th treatment he was verbally responsive but 4 months of rigidity & forced bed rest had left him with limb contractures and such badly impaired movements that he was unable to stand or use his hands to feed himself. Both catatonia and psychosis were relived After 22 ECT he was transferred to rehabilitation center and 4 months later he was again able to walk, use his hands and care for himself. COMMENTS This patient s ordeal was prolonged by several clinical missteps. Persisting in a failed trial with bromocriptine and dantrolene was not correct Generally if an acutely ill patient has not improved substantially within 7-10 days of treatment, that treatment needs to be reconsidered and probably changed Catatonic features interfering with general medical health, even catatonic features attributed to antipsychotic drugs improve substantially within several days when properly treated For this patient inadequate nursing care allowed contractures to develop The unavailability of ECT at a tertiary care hospital was indefensible. A long ill catatonic patient with joint contractures was successfully treated with Acts. REFERENCE: Mashimo et al 1995 quoted in Catatonia by Fink and Taylor 2003 Cambridge University press; pp th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 4

6 Catatonia is one clinical condition which reminds us that patients do not follow books but books are written by following patients 15th, January 2007 Amresh Srivastava, 5

7 Catatonia: A life threatening condition. A syndrome Catatonia is currently considered to be a psychomotor syndrome Remarkable constellation of motor and behavioral signs and symptoms that often occurs in relation to neuromedical insults. Structural brain lesions, intrinsic brain disease, and other systemic disorders that affect the brain, as well as idiopathic psychiatric disorders have been found to be associated 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 6

8 Catatonia: Historical evolution Catatonia or tension Insanity- Kahibaum 1874 Catatonia-dementia praecox kraeplin 1899 Symptoms as manifestation of Freudian complexes-bleuer 1911 With MDP - kahlbaum 1874 Motility Psychosis-Wenicke 1900 Cycloid Motility psychosis- Kleist 1912 and leonhard 1957 Catatonic schizophrenia-a group of Cerebral System Disorder - Kleist 1923 In Childhood & adolescence- Raecke 1909 Catatonia & Hysteria-Charcot 1886 Catatonia & OCD-Bleuler 1911,Kruger 2000 It was also well known that it could occur secondary to neurological, toxic-metabolic and infectious etiologies. Identified exclusively with schizophrenia as late as DSM III/ III-R This limitation changed in DSM-IV. 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 7

9 Epidemiology ( definition & concept) 1.rates of catatonia- a) General psychiatric Condition hospitalized acute psychosis b) mood disorder % c) schizophrenia- 6% in 1850 & 0.5% in 1950 incidence of catatonia % decrease 28.8 change in diagnosis time scale % decrease in incidence at one site diagnosis 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 8

10 Nosology Motility psychosis Catatonic schizophrenias A- unsystemetic catatonic, schiz, periodic catatonia B-systematic- schizophrenias 1.Para kinetic 2.mannerist Pros kinetic Negativistic Speech prompt Speech inactive Nosologic validity continues to be debated Concept & descriptive psychopathology-still insufficient Study of catatonia can be advanced by-- Adopt the approach of catatonia across psychiatric illness Reject notion of subtype or modifier Postulate as separate entity 15th, January 2007 Amresh Srivastava, 9

11 Current phenomenological classification As per DSM-IV; Now it is categorized as Catatonic disorder due to general medical condition Mood disorder with catatonic features The catatonic type of schizophrenia. Historically, Pre and post neuroleptic era has been found strongly associated with incidence of catatonia. Psychogenic catatonia Neuroleptic induced catatonia -NMS [ catatonia preceding NL administration and developing into NMS] Are possibly most suitable clinical classification. 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 10

12 Catatonia in psychiatric classification: the evidence Catatonia is a condition qualifying for finding its own place in various diagnostic systems. Because:- Catatonia is common Is Identified as a syndrome Can be Delineation from other syndromes[ differential diagnosis] Catatonia is also known by by other names Known to have Good response to specific treatment Common causes of catatonia Mood disorder General medical and neurological conditions Non-affective psychosis Genetic form of catatonia 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 11

13 Proposed category for classification Max Fink & Taylor; 2003 DSM Code xxx.0 Catatonia Code.xxx.1 Nonmalignant catatonia Code.xxx.2 delirious catatonia Code.xxx.3 malignant catatonia,nms, serotonin syndrome Specifier Code.xxx.x1 secondary to mood disorder Code.xxx.x2 secondary to gen.med.condition Code.xxx.x3 secondary to neurological dis. Code.xxx.x4 secondary to psychiatric disorder 15th, January 2007 Amresh Srivastava, 12

14 Proposed diagnostic criteria Max Fink & Taylor; 2003 A.immobility,Mutism,or stupor of at least 1 hours duration,associated with at least one of the followings: catalepsy,autonomic obedience,or posturing,observed or elicited,on two or more occasions. B.in absence of immobility,mutism or stupor,at least two of the followings:stereotypy,echophenomena,catalepsy,aut onomic obedience,posturing,negativism,gagenthalten, ambitendency 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 13

15 Catatonia & NMS {NL induced catatonia}, a lethal and malignant syndrome with high mortality-nms : first description 1960 by Delay et al. Share a common pathophysiology,& clinical manifestation While most cases of catatonia do not meet criteria for NMS, all unequivocal cases of NMS appear to meet criteria for catatonia. Though the syndrome has been described in different times, there is remarkable amount of similarity 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 14

16 The classical features of catatonia: about 42 symptoms have been identified Catatonia has three groups of symptoms: motor symptoms behavioral symptoms emotional symptoms All three have different underlying pathophysiological mechanism Mutism Immobility Staring Posturing Negativism Withdrawal 15th, January 2007 Amresh Srivastava, 15

17 Subtypes and classification: Main subgroups are: Malignant and Non-malignant Catatonia Catatonic withdrawal Catatonic excitement Alternating Periodic [ excitement alternating with stuperous state] Lethal catatonia Catatonic stupor Malignant Simple - nonmalignant Pernicious NMS variants Clinical description, course and outcome 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 16

18 Catatonia : Idiopathic: without brain atrophy & -with brain atrophy Associated with bipolar disorder; major depression other affective disorder: schizophrenia; other psychiatric disorder [Psychogenic] Catatonia secondary to:( Medical Catatonia) TLE other Seizure Disorder brain tumor brain trauma encephalitis- post encephalitis state cerebro vascular diseases focal brain lesions akinetic mutism Parkinson's Toxic encephalopathy Metabolic encephalopathy Other medical disorders NMS Neuroleptics Other prescribed psychotropics Illicit psychotropics Phencyclidine exposure, SLE, Corticosteroids; disulfiram Porphyria 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 17

19 Assessment of catatonia by Braunig catatonia rating scale The scale contains 21 items (16-motor symptoms & 5 behavioral symptoms rated from 0-4) Motor excitement Verbigeration Stereotypis Motor inhibition Iteration Grouping Impulsivity Mutisim Grimacing Exaggerated responsiveness blinking Mannerism Gerky movements Genhalten Rigidity Negativism Parakinesis Postural Waxy flexibility Rituals Automatic obedience Mood disorder vs. schizophrenia 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 18

20 Catatonic spectrum disorders: depending upon shared neurobiology Lethal malignant catatonia - high mortality NL induced catatonia, NMS, Serotonin syndrome Classical catatonic stuperous state Various independent catatonic symptoms Catatonia variants Non-malignant simple catatonia Autism spectrum disorder 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 19

21 Incidence of catatonic schizophrenia in various countries 40% 35% 30% 25% has reduced over time due to several factors, generally observed in about 10-15% of psychiatric population;4% TO 10% IN ACADEMIC INPATIENT UNITS 20% 15% 10% 5% 0% Germany U.S. Germany U.S. U.S. U.S. U.S. India U.S. Countries 15th, January 2007 Amresh Srivastava, 20

22 Are we witnessing the disappearance of catatonic schizophrenia? Symptoms or syndrome.?? E.Bleuer 1991 >33 Kraepelin Mayor-Gross Leonhard Leonhard Astrup fish Huber Huber M.Bleuer Muller Warthen Morrison Kasper Strass Kane Stieglitz th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 21

23 feature Catatonia in depression motoric immobility stupor;extreme agitation;extreme negativism;posturing;stereotyped movements,mannerisms,or grimacing and echolalia or echopraxia treatment BZ with continued oral administration, When, no relief, urgent provision for ECT After catatonic symptoms are relieved Tx should continue with ADD,Lithium, APD or combination outcome Efficacy of ECT usually appears after few treatments, ECT may initially be administered daily 15th, January 2007 Amresh Srivastava, 22

24 features Catatonia in mania develop in 1/3 of patients. are--motor excitement,mutism,and stereotypic movements,patients exhibiting stupor may go on to show more typical signs of mania, greater episode severity,mixed states,and poorer short-term outcome, treatment outcome Lorazepam is effective, ECT is most effective,regardless of etiology,should be considered if BZ fails. NL generally have exhibited poor efficacy, Leonhard: 2 types of MDP with catatonic features;with or without catatonia;significantly differing on mean number of days in hospital 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 23

25 High risk or At-risk or Vulnerable for catatonia & poor prognosis Male gender Adolescent onset Presence of autistic traits Obstetric events Post-natal brain insult Soft neurological signs NL sensitivity Family history of catatonia Catatonia generally has good outcome but presence of catatonic symptom has poor prognosis of schizophrenia or mania 15th, January 2007 Amresh Srivastava, 24

26 NMS & its Risk factors Mortality has decreased from 20% to 10% and incidence has also decreased. Life time incidence - about 0.2% amongst antipsychotic users Hyperthermia and rabdomyolysis may lead to renal failure CPK rises dramatically [ even up to 60K units] Risk factors include:- Rapid dose escalation of HP, first generation APD Parenteral administration of APD Underlying neurological impairment NMS is probably less common with second generation APD than with first one. Incidence with first generation is low now possibly because of low dosage than in the past. Polypharmacy, concomitant anticholinergics,lithium 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 25

27 NMS & its Risk factors May be fatal, if untreated, Tx. Includes : temperature control by cooling,fluid correction,da agonist-bromcriptine 2.5 mg QDS, muscle relaxant, dantrolene mg/kg,iv 6 hourly ECT is indicated if catatonia related to NMS persists or response is inadequate with drugs, Need for APD should be carefully assessed, before resumption, When another trial of APD is attempted, second generation, particularly clozapine are preferred, A re-challenge should begin with low dose and slow titration 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 26

28 NMS variables Death Sequelae Full recovery N=17 N=10 N=22 age female 59% 60% 23% Psychomotor excitement 41% 60% 36% dehydration 54% 80% 64% Lithium 18% 30% 9% Antiparkinsons 76% 30% 77% I/M NL 35% 30% 14% Dose NL/day Loading dose NL/d dantrolene 59% 80% 59% bromcriptine 14% 30% 41% Max CPK 1000 IU/L th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 27 Max body temperature

29 Differential Diagnosis organic,psychogenic,drug induced, idiopathic, Idiopathic primary catatonia Secondary catatonia Lethal catatonia Catatonic excitement Diagnosis is essentially clinical supported by measurement and rating scales, Rule out other causes presents as emergency, move very quickly and systematically Often diagnosing catatonia in schizophrenia vs. mania is difficult at the beginning. 15th, January 2007 Amresh Srivastava, 28

30 Clinical dilemmas and challenges Very severe cases has less problem, Most of the difficulties arise in borderline cases. New contact : most would adopt rule out. Time length for definitive Tx is crucial Severe excitement is a management problem Partial syndromes only When diagnostic criteria is not fulfilled Presence of high fever and h/o NL Rapid cycling and periodic catatonia When response does not progressed 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 29

31 Clinical dilemmas and challenges When response does not sustain Frequent relapses Determining psychiatric diagnosis schizophrenia vs. mood disorder Presence of psychosis; Use Antipsychotic ; to be or not to be Should CSF be checked / routinely Deciding about ECT in medically compromised Therapeutic or service set up Issues of transfer Issues around consent and capacity 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 30

32 Clinical dilemmas and challenges Late onset, paediatric, in pregnancy Planning relapse prevention Which antipsychotic in catatonic Schizophrenia after termination with ECT and which MS and ADD in Bipolar Disorder? Virtually all APD typical or atypical have been known to cause NMS,Incipient NMS or its variants, including clozapine. All atypical APD have shown some degree of response in NMS and catatonia? Clinical guidelines are not clear and experience is the best guide. 15th, January 2007 Amresh Srivastava, 31

33 APA practice Guidelines there are at present no treatment strategies specific to the various subtypes [ of schizophrenia] with exception to the use of BZ for Catatonia In Mania use BZ and ECT In depression; concurrent ADD use and BZ with ECT, after catatonic features are relieved TX may be continued with ADD,Lithium,APD or a combination.. 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 32

34 Special conditions Catatonia-autism spectrum Catatonia in childhood and adolescence Late-onset catatonia Catatonia in liver transplant Post-partum catatonia Catatonia in co-morbid medical condition like hypertension 15th, January 2007 Amresh Srivastava, 33

35 Clinical advances Catatonia is an infrequent but severe condition in young people, and is usually associated with schizophrenia. Obstetric complications and neurological abnormalities in neuroleptic-naive psychotic patients. Blueprints for the assessment, treatment, and future study of catatonia in autism spectrum disorders. Shared susceptibility region on chromosome 15 between autism and catatonia. Classification matters for catatonia and autism in children. NMS in adolescents after brief exposure to olanzapine Catatonia in Alzheimer's Lewy body dementia after Donapezil Malignant and late onset catatonia Catatonia after single dose of ecstasy 15th, January 2007 Amresh Srivastava, 34

36 Relative Prognosis Best Better Good poor mood disorder without catatonia depression With catatonia periodic catatonia cycloid psychosis with catatonia Bipolar disorder with catatonia catatonic schizophr enia noncatat onic schizoph renia. 15th, January 2007 Amresh Srivastava, 35

37 Fundamental Problem A disorder of Motivation and Movement link Catatonic patients are well able to initiate movements, but they are apparently unable to terminate the movement once initiated in an appropriate way. In contrast to initiation, neural network study of underlying termination of movement has been neglected in the research to date. 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 36

38 All information put together, it appears that the Motor symptoms nigrostriatal, basal ganglia and motor cortex Emotional symptoms ---- prefrontal and limbic cortex Behavioral symptoms---mesolimbic cortex All three are interdependent because of circuits and loops which are closed within these structures. That there is a pre-existing brain insult present in vulnerable candidates 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 37

39 Various hypothesis have been proposed. Neurotransmitter hypothesis Universal field hypothesis Vulnerability theory because of brain structural changes Emotional-motor activation paradigm Motivation-movement paradigm Neurochemical: increased CPK and Low serum Iron Neuronal Circuits paradigm Restitutive dopamine hypothesis Top-down modulation : A Neuropsychiatric hypothesis: parallel from Parkinson's disease 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 38

40 Dopamine hypo-activity There is dysfunction in neurotransmission in cortical and subcortical areas. The dysfunction is a result of a combination of NT involvement. Leading NT involved are DA,GABA,5HT,NMDA There is hypofunction D2 activity in various cortical areas mesolimbic, nigrostriatal, motor, prefrontal and orbitofrontal areas Decreased D2 function is also found in caudate nucleus, nucleus accembens, palladium and thalamus. This hypothesis proposes that it is the interaction of these systems that predisposes, initiates, and maintains the twin syndromes of catatonia & NMS 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 39

41 Catatonia is a delicate balance between dopamine and Gaba neurons Major NT NMDA DA, GABA, NMDA, 5HT2a Gaba-A Gaba-B--ratio decreased 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 40

42 Gaba and major brain areas The ratio of GABA A and GABA B may play a role in development of catatonia. There is Hypo activity at GABA A receptor; Lorazepam, a GABA agonist is effective in catatonia Serotonin Hyperactivity at the 5-HT 1A receptor hypo activity at 5HT 2A receptor Glutamate Hypo function of NMDA Receptor Major Brain regions implicated in catatonia are: Limbic system - nucleus accumbens Thalamus Caudate nucleus Motor area Fronto-orbito cortex Right posterior parietal cortex Mesolimbic and mesostriatal cortex, 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 41

43 DA GABA 15th, January 2007 Amresh Srivastava, 42

44 catatonia Findings of brain imaging Structural changes Neuropathological findings Functional changes Caudate Nucleus:Palladium; nucleus accembens;thalamus shows Decreased cell density reduced activity in medial orbitofrontal cortex during negative emotional stimulation,suggesting possible initiation point. imaging and neuropsychology indicate a relationship between deficits in visual-constructive function & decreased rcbf in the right posterior parietal cortex, alteration in right posterior parietal function may count for the deficit in termination of movements responsible for motor symptoms of posturing. 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 43

45 Movement control In healthy individuals termination of movement involves. the right posterior parietal cortex because the registration. on line monitoring of the respective spatial position of the movement may be of central importance for an appropriate termination. Negative emotional processing in the right medial orbitofrontal cortex may be particularly altered in catatonia with an abnormal functional connectivity to the premotor/motor cortex 15th, January 2007 Amresh Srivastava, 44

46 Neuronal circuits and catatonia Cognitive,behavioral and emotional circuits Each circuit has cortico/limbic, striatal, pallidial/nigral, and thalamic nodal points with the loops closed by thalmocortical connections. Any neuromedical or psychiatric disturbance significant enough to disrupt the GABA-DA balance in the mesotriatal-mesocortocolimbic medial forebrain bundle of DA tracts with terminal fields in nucleus accumbens, the anterior cingualte, and the prefrontal cortex system anywhere along the circuitry will potentially set off a catatonic response. 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 45

47 15th, January 2007 Amresh Srivastava, 46

48 Dopamine restiturive hypothesis DAgic system in involved in protecting against the emergence of psychotic symptoms, DA-gic system then may stabilize mental homeostatic by spontaneous Down regulation of its own function In some patients, this down reg. is sufficient to maintain a non-psychotic state if the biological or psychological stresses are so severe that down regulation is not adequate to prevent psychosis. The syndrome appears Periodic catatonia: confirmation of linkage to chromosome 15 and further evidence for genetic heterogeneity. Periodic catatonia is the first sub-phenotype of schizophrenic psychoses with confirmed linkage despite the existence of considerable genetic heterogeneity. 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 47

49 Top-down modulation : A Neuropsychiatric hypothesis Differential diagnosis of motor symptoms is difficult. Symptoms may have CNS origin [Parkinson's] or psychiatric [ catatonia] Despite differences in origin symptoms may appear similar Possibility of dissociation between origin and clinical appearance may reflect functional brain organization in general & cortical-cortical/subcortical in particular. hypothesized : similarities and differences between Parkinson's disease and catatonia - accounted for by distinct kind of modulation between cortico-cortical and cortico-subcortical relation. The different symptoms be accounted for by dysfunction in orbitofrontalprefrontal/parietal cortical connectivity reflecting horizontal modulation of cortical-cortical relation. reflecting vertical modulation of caudate and other BG by GABAergic mediated orbitofrontal cortical deficit may account for motor symptoms in catatonia. 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 48

50 Modulation OFC Pre Frontal - + Motor & Pre-motor cortex Horizontal BG Vertical Or Top-down 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 49

51 Issues about management Over time the mortality has decreased Needs emergency and multidisciplinary care Often requires Intensive care team Management focus has to be on 1. Establishing the diagnosis asap.2. Arrange supportive treatment,3.rule out secondary causes.4consider definitive treatment,all without loss of time Clinical presentation is rarely uncomplicated Duration of untreated illness is very high. 15th, January 2007 Amresh Srivastava, 50

52 Management Thus complications of nutritional deficiency,starvations, posturing, metabolic imbalance,infection,worm infestation,skin diseases,injury, cardiac complication,fever and toxemia are common. Thus management should address:- Vital functions, nutrition, hydration, correction of electrolyte,infection and other relevant condition, and Then proceed for definitive treatment with BZ,ECT etc. Fitness to anaesthesia and ECT is a crucial clinical issue. 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 51

53 Treatment options Electroconvulsive therapy and lately benzodiazepines are not only effective treatment options in this form of catatonia,but also helped generate neurobiological hypotheses concerning its pathophysiology LORAZEPAM IV CHALLENGE IF POSITIVE, LORAZEPAM ORAL. DOSAGES ARE HIGH MG/DAY ECT DAILY TREATMENT FOR 2-5 DAYS BILATERAL ELECTRODE PLACEMENT AVOID ANTIPSYCHOTIC DRUGS 15th, January 2007 Amresh Srivastava, 52

54 Catatonia rating Treatment of catatonia with IV lorazepam Prospective Study : Bush et at., DOSES AT 5 MIN INTERVAL N=9 0 0 BASELINE TX - 1 TX - 2 POS RESP NON RESP Ungvari : demonstrated that lorazepam was not effective in chronic states of catatonia, associated with chronic psychiatric conditions.---- suggesting that not all catatonia are lorazepam - responsive 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca POS RESP 2 NON RESP

55 Tx of associated Disorder.e.g. Psychotic/bipolar AATPD Catatonia Supportive & preventive measures Atypical APD Evidence from Case reports And retrospective chart Review Caution: NMS Non-Malignant Catatonia BZ low dose BZ High dose MC / NMS BZ/ ECT approach OR DA -muscle relaxant approach Stop classical antipsychotic No indication of atypical APD BZ High dose ECT ECT 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 54

56 Treatment of Catatonia A. simple catatonia(including NLinduced catatonia) Lorazepam Still catatonic DA Agonist Still catatonic ECT B.lethal catatonia (including NMS) Lorazepam And/or DA agonist +/- Dantrolene Still catatonic ECT - prior to 5 days Valproate for catatonia: need for caution in patients on SSRIs and antipsychotic. 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 55

57 Advances in management meantime, may be beneficial in catatonic schizophrenia due to a glutamatergic dysfunction present in catatonic patients. Clozapine monotherapy for catatonic schizophrenia: should clozapine be the treatment of choice, with catatonia rather than psychosis as the main therapeutic index? Clozapine withdrawal catatonia associated with cholinergic and serotonergic rebound hyperactivity: a case report. Medical complications of catatonia: a case of catatonia-induced deep venous thrombosis. Gilles de la Tourette form of catatonia: response to ECT. Catatonia and transcranial magnetic stimulation. Lethal catatonia responding to high-dose olanzapine therapy. Lithium carbonate in prophylaxis of reappearing catatonic stupor: case report. Treatment of catatonic syndrome with fluoxetine. Case report] 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 56

58 Advances: future questions Nonconscious processing, anterior cingulate and catatonia Catatonia is not ready for unified theory Does catatonia has a specific brain biology What medical catatonia tell us about top down modulation Catatonia- a window into the cerebral underpinnings of will Catatonia-a disorder of motivation and movement Cognitive-motor deficit in catatonia 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 57

59 Finally, its clear that 1.our conceptualization of catatonia has changed over years away from a motor manifestation of schizophrenia and towards a motor,behavioural, emotional manifestation of mixed mania and many other organic disorders its patho-physiology continues to be a mystery. 3. however it is an important clinical syndrome and still continues to be life threatening condition in neuropsychiatry 15th, January 2007 Amresh Srivastava, asrivas9@uwo.ca 58